Low frequency neurostimulator for the treatment of neurological disorders

ABSTRACT

A system for treating neurological conditions by low-frequency time varying electrical stimulation includes an electrical device for applying such low-frequency energy, in a range below approximately 10 Hz, to the patient&#39;s brain tissue. An implantable embodiment applies direct electrical stimulation to electrodes implanted in or on the patient&#39;s brain, while a non-invasive embodiment causes a magnetic field to induce electrical currents in the patient&#39;s brain.

CROSS-REFERENCE TO RELATED APPLICATIONS

This is a continuation of U.S. patent application Ser. No. 15/137,670,filed Apr. 25, 2016, now U.S. Pat. No. 9,694,195 which is a continuationof U.S. patent application Ser. No. 14/688,935, filed Apr. 16, 2015, nowU.S. Pat. No. 9,352,168, which is a continuation of U.S. patentapplication Ser. No. 12/549,303, filed Aug. 27, 2009, now U.S. Pat. No.9,033,861, which is a continuation of U.S. patent application Ser. No.11/436,676, filed May 16, 2006, now U.S. Pat. No. 7,601,116, which is acontinuation of U.S. patent application Ser. No. 10/245,992, filed Sep.17, 2002, now abandoned, which is a divisional of U.S. patentapplication Ser. No. 09/652,964, filed Aug. 31, 2000, now U.S. Pat. No.6,591,138.

BACKGROUND

Technical Field

This invention is in the field of devices for the treatment ofneurological disorders in human subjects, particularly those disordersthat originate in the brain.

Background

The current state of the art in treating neurological disorders such asepilepsy or Parkinson's disease involves either drugs, destructivenigral lesions or the open-loop electrical stimulation of neurologicaltissue. Drug therapy has been shown to have significant short andlong-term side effects and is often ineffective. In U.S. Pat. No.3,850,161, Liss describes a continuous closed-loop feedback system whichwill always feedback part of the brain EEG signal to separate electrodesso that if a large EEG signal occurs it will be fed back in an attemptto cancel out the original signal. The system does not take advantage ofrecently developed digital signal processing and microcomputertechnology by which feedback signals can be activated only when aneurological event occurs, nor does it provide a practical way torecognize and intervene during early stages in the evolution of aneurological event. In addition, the Liss device is not programmable andit does not provide any capability to record EEG signals. Examples of a“neurological event” are the occurrence of an epileptic seizure, atremor or the occurrence of a migraine aura or migraine headache. A“neurological event” is defined herein as either the precursor of anevent such as an epileptic seizure, or the event itself. This concept ofdetecting an electrical precursor that is a first type of neurologicalevent that occurs some time before the “real” event (i.e. anomalousbrain electrical activity or a particular pattern of neural activityassociated with clinical symptoms) is an important aspect of the presentinvention. It has been shown that both epileptic seizures andParkinson's tremors have precursors that occur before and can be used topredict the onset of the clinical symptom. It is also very likely thatother neurological events such as migraine headaches and depressionwould have anomalous electrical activity predictive of the onset ofclinical symptoms. Methods for prediction of epileptic seizures havebeen published by Elger and Lehnertz (in Elger, C. E., and Lehnertz, K.,“Seizure prediction by non-linear time series analysis of brainelectrical activity,” Eur. J. Neurosci. 1998 February; 10(2): 786-9, andOsorio, Frei and Wilkinson (in Osorio, I., et al., “Real-time automateddetection and quantitative analysis of seizures and short-termprediction of clinical onset,” Epilepsia 1998 June; 39(6): 615-27.

Maurer and Sorenson in U.S. Pat. No. 4,019,518 describe a combinedinternal/external system for electrical stimulation of the body withbiphasic pulses but do not describe any means of detecting neurologicalevents. Fischell in U.S. Pat. No. 4,373,527 describes a programmablemedication infusion system but does not anticipate its use in responseto a detected neurological event.

More recently, a device has been approved for human use to stimulate thevagus nerve in a continuous fashion with the objective of decreasing therate of epileptic seizures. Clinical reports on such devices indicateonly a modest degree of success in that only 50% of the patientsexperience a greater than 20% reduction in the rate of epilepticseizures. Another device that has been recently introduced into clinicalpractice utilizes intermittent or continuous stimulation of the thalamusfor the treatment of involuntary motion disorders such as Parkinson'ssyndrome. Neither of these two open-loop devices described above ishighly effective for the treatment of a neurological disorder such asepilepsy, and neither anticipates the use of decision making in order tooptimize a response to terminate the precursor of a neurological eventor the neurological event itself; nor does either device allow for therecording of EEG signals. In addition, both known devices usestimulation frequencies above 10 Hz, which for the reasons set forth indetail below, are not optimal.

Fischell et al in U.S. Pat. No. 6,016,449, which is incorporated hereinby reference, teaches a fully implantable neurostimulator capable ofresponsive treatment of neurological disorders. However, Fischell doesnot discuss in detail the advantageous use of low frequency stimulationas a means of inhibiting epiliptiform activity.

It is well known that slow wave potentials in the brain are ofteninhibitory in nature yet all known stimulation attempts to treatepilepsy in humans have used relatively high frequency stimulation, inmost cases greater than 20 Hz. These higher frequencies, while effectivefor a brain mapping type procedure, have significant potential to induceepileptogenic activity. In fact, Hallett in “Transcranial magneticstimulation and the human brain,” Nature, Vol. 406, 13 Jul. 2000, statesthat while “rapid repetitive transcranial magnetic stimulation (rTMS),at frequencies of 5 Hz and higher, will transiently enhance motorexcitability . . . slow rTMS, at 1 Hz will transiently depressexcitability.”

SUMMARY

There is good evidence that slow wave activity is inhibitory in thecentral nervous system of man (Staton, R. D. et al., “Theelectroencephalographic pattern during electroconvulsive therapy: V.Observations on the origins of phase III delta energy and the mechanismof action of ECT,” Clin. Electroencephalogr. 1988 October; 19(4):176-198 and animals (Buzsaki, G. et al., “Depth profiles of hippocampalrhythmic slow activity (‘theta rhythm’) depend on behaviour,”Electroencephalogr. Clin. Neurophysiol. 1985 July; 61(1): 77-78)including such stimulation applied to the hippocampus (Leung, L. S. etal., “Theta-frequency resonance in hippocampal CAI neurons in vitrodemonstrated by sinusoidal current injection,” J. Neurophysiol. 1998March; 79(3): 1592-6). These slow waves may be at theta frequencies (4to 7 Hz—Buzsaki et al. 1985), delta frequencies (1 to 3 Hz—Staton et al.1988), or even at less than 1 Hz (Contreras, D. et al., “Cellular basisof EEG slow rhythms: a study of dynamic corticothalamic relationships,”J. Neurosci. 1995 January; 15(1 Pt 2): 604-22). Paatta et al. (in“Control of chronic experimental focal epilepsy by feedback caudatumstimulation,” Epilepsia 1983 August; 24(4): 444-54) describe successfulictal spike depression by 5 Hz stimulation of the caudate nucleus (CN)in cat brains. The article also states that stimulation of the thalamus,mesencephalic reticular formation or hypothalamus was not effective.Finally, Hallett (in “Transcranial magnetic stimulation and the humanbrain,” Nature 2000; 406 (July 13): 147-150) discusses the inhibitoryeffects of low frequency pulsing from a transcranial magneticstimulator.

The present invention includes transcranial stimulation, or direct brainstimulation from multiple electrodes, in either an open or closed-loopsystem for the treatment of certain neurological disorders such asepilepsy, migraine headaches and Parkinson's disease. A purpose of thepresent invention is to overcome the shortcomings of all known devicesfor the treatment of such disorders. Specifically, the present inventionutilizes slow wave potentials (low frequency stimulation in a range ofapproximately 1 to 10 Hz) to prevent or abort a neurological event.

One embodiment of the present invention envisions a multiplicity ofbrain electrodes placed either within the brain, on the surface of thebrain itself, or on the dura mater that surrounds the brain. Some or allof these brain electrodes may be used to directly detect an abnormalneurological event such as an epileptic seizure, or they may be used todetect a pattern of electrical activity that precedes or accompanies anabnormal neurological event. A stimulation signal can also be applied toany one, several, or all elements of such an electrode array. Thestimulation signals sent to each electrode may be identical or they maybe programmed to differ in amplitude, frequency, waveform, phase andtime duration. It is also envisioned that sensing electrodes may beentirely separate from the electrodes used for responsive stimulation.

It is also envisioned that appropriate selection (i.e., location) ofelectrode sites can be used to enhance the reliability for detection andtermination of a neurological event. Thus, the present inventionenvisions enhancement of detection by the use of the spatial domain asit applies to the positioning of detection and treatment electrodes.

A specific capability of this system is to provide electricalstimulation to a specific portion of the brain as the means of stoppinga neurological event. It is believed that the earliest possibledetection of a seizure and treatment of aberrant electrical activityfrom an epileptic focus has the highest probability of aborting theoccurrence of a full seizure. It is envisioned that either throughspecific placement of treatment electrodes or by adjusting the phase ofsignals applied to an array of electrodes, stimulation can be directedto the locations(s) within the brain that offer the highest probabilityof stopping the seizure. Detection of an abnormal neurological eventwould allow detection of specific but apparently normal patterns ofelectrical activity, which are reliable producers of the abnormal event;stimulation during the appearance of such patterns may prevent theoccurrence of the event.

A novel aspect of a preferred embodiment of this invention is that theentire implantable portion of this system for treating neurologicaldisorders is implanted under the patient's scalp or intracranially. Suchplacement will either have the device located between the scalp and thecranium or within a hole in the cranium. Because of size constraints,the intracranial location is the preferred embodiment.

The implantable portion of the system includes: (1) electrodes that liein close proximity to or actually within the brain, (2) a control modulethat contains a battery and all the electronics for sensing, recordingand controlling brain activity, (3) electrically conducting wires thatconnect the control module to the electrodes, (4) a buzzer providing anacoustic signal or electrical “tickle” indicating that a neurologicalevent has been detected, and (5) an input-output wire coil (or antenna)used for communication of the implanted system with any and all externalequipment. The battery that provides power for the system and anelectronics module are both contained within a metal shell that lies, inone embodiment, under the patient's scalp. The metal shell, whichcontains the electronics module and the battery collectively, forms thecontrol module.

All electrodes connect by way of electrically conducting wires toelectrical terminals that are formed into the metal shell. Theelectronics module is electrically joined to the brain electrodes by wayof the shell's electrical terminals, which are electrically joined tothe wires that connect to the brain electrodes.

An important aspect of the preferred embodiment of this device is thefact that the shell containing the electronics module and the battery,i.e. the control module, is to be placed in the cranium of the skull ata place where a significant volume of bone is removed. By placing theentire system within the cranium, (as opposed to having some wiresextending into or through the patient's neck to a control module in thechest) the probability of wire breakage due to repeated wire bending issignificantly reduced. However, the present invention also envisions theplacement in the chest or abdomen of a control module if a large batteryor a large volume electronics module dictates such a large size for thecontrol module that it cannot be conveniently placed within the cranium.Such a thoracic or abdominal placement of a control module wouldtypically require wires to be run through the patient's neck.

The present invention also envisions the utilization of an intracranialsystem for the treatment of certain diseases without placing wiresthrough the neck. Specifically, an alternative embodiment of theinvention envisions the use of electrodes in or on the brain with anintracranial control module used in conjunction with a remotesensor/actuator device implanted elsewhere in the patient's body. Forexample, blood pressure could be sensed with a threshold or, forexample, 150 mm Hg, and if that pressure is exceeded, a signaltransmitted by electrical conduction through the body from the remotesensor/actuator device could be received at the control module, whichwould initiate brain stimulation in such a way as to reduce the bloodpressure. Conversely, if the brain perceives pain and generates acorresponding signal detectable by the intracranial control module, asignal could be sent by electrical conduction through the body to theremote sensor/actuator device, which would provide responsive electricalstimulation to locally stimulate a nerve, thereby reducing theperception of that pain. In still another embodiment, if a precursor ofan epileptic seizure is detected, the remote sensor/actuator could beused to electrically stimulate one or both vagis nerves so as to stopthe epileptic seizure from occurring. Such a remote device could belocated in the trunk of the patient's body. In an embodiment of theinvention, a remote sensor/actuator may be used to deliverinstantaneous, intravenous, intraperitoneal, subdural orintraventricular (of the brain) therapeutic chemicals, includingmedication, neurotransmitters and ionic substances, alone or inconjunction with electrical stimulation. Such a remote sensor/actuatoris disclosed in the above referenced U.S. Pat. No. 6,016,449 by Fischellet al.

It is also envisioned the ideal stimulation to prevent or abort aneurological event has a low frequency (e.g., 1 to 8 Hz) that wouldresemble slow wave inhibitory potentials and be significantly lesslikely to induce epileptiform activity. In one embodiment of theinvention, the stimulation waveform is substantially sinusoidal and hasminimal higher-order harmonics, and hence little energy above thefundamental frequency. In an alternative embodiment, the low frequencystimulation comprises a sequence of short duration biphasic pulseshaving a repetition rate of less than about ten pulses per second (10Hz). Such stimulation could be applied to the caudate nucleus or otherstructures of the brain, including the hippocampus. As patientssuffering from Parkinson's have an extremely low incidence of epilepsyand one manifestation of Parkinson's is characterized by a 5 Hzelectrical oscillation that begins in the Thalamus, it is conceived thatlow frequency stimulation of the Thalamus could, in fact, be inhibitoryto epileptiform activity. Such stimulation could be responsive to thedetection of a precursor to a clinical seizure or the epileptiformactivity from the seizure itself. Alternately, periodic slow wavestimulation applied without detection could prevent the brain fromgenerating seizure activity. Although epilepsy is currently believed tobe the most applicable use of such slow wave stimulation, it could alsobe successful for migraines, pain, tremor, Parkinson's, depression orother neurological disorders.

It is also envisioned that while the standard treatment would have aconstant amplitude for the duration of the low frequency stimulation, itmay be advantageous to have the amplitude begin high and decrease overthe duration, begin low and increase over the duration, or varyaccording to any desired treatment plan. The typical duration of lowfrequency stimulation that would be used to stop a neurological eventwould be between 100 ms and 10 seconds.

Another embodiment of the present invention that would be significantlyless invasive involves the use of Transcranial Magnetic Stimulation(TMS) from an external coil TMS stimulator. Such a device could beincorporated into a bicycle type helmet and could be used at the time apre-event aura is sensed by the patient. Alternately, such an externalsystem could be used in a repetitive or continuous mode for patientswith serious disorders who often wear protective helmets. A TMS devicecould be extremely effective if it is pulsed on and off at frequenciesbelow 10 Hz.

Thus it is an object of this invention to provide appropriate slow wavestimulation of the human brain in response to a detected neurologicalevent in order to cause the cessation of that neurological event. Thepattern and frequency of stimulation can be modified to provide optimalcontrol of the unwanted neurological event in each patient.

Another object of this invention is to use periodic slow wavestimulation of the brain to treat neurological disorders.

Another object of the invention is to use continuous slow wavestimulation of the brain to treat neurological disorders.

Still another object of this invention is to have a system of electrodesconnected by wires to a control module, the entire system being placedunder the scalp or intracranially, and being substantially containedwithin an opening in the cranium.

Still another object of this system is to have essentially no flexure ofinterconnecting wires so as to enhance system reliability.

These and other objects and advantages of this invention will becomeapparent to a person of ordinary skill in this art upon careful readingof the detailed description of this invention including the drawings aspresented herein.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a top view of a human head showing the configuration of animplantable system for the treatment of neurological disorders as itwould be situated in the human skull.

FIG. 2 is a block diagram of the implanted and external portions of thesystem.

FIG. 3 is a cross section of an embodiment of the present inventionshowing a magnetic depolarizer system within a helmet on the head of apatient.

FIG. 4A is a longitudinal cross section of the magnetic depolarizer.

FIG. 4B is a top view of the magnetic depolarizer.

FIG. 5 is a simplified circuit diagram of the main components of amagnetic depolarizer system.

DETAILED DESCRIPTION

FIG. 1 illustrates the configuration of an implantable system 10 for thetreatment of neurological disorders as it would be situated under thescalp of a human head 9, the system including a control module 20,electrodes 15A, 15B, 15C, 15N and 16 with wires 17A, 17B, 17C, 17N and18 connected through a connector 8 to the control module 20. It isenvisioned that the control module 20 is permanently implanted into thetop of the patient's skull in a location where the skull is fairlythick. It is also envisioned that the control module 20 could be locatedin the trunk of the patient's body like a heart pacemaker with theconnecting wires being run through the patient's neck, under thepatient's skin or otherwise. Each of the electrodes 15A, 15B, 15C, 15Nand 16 would be placed under the cranium and above the dura mater (i.e.,placed epidurally) or placed deep into the brain. The connecting wires17A, 17B, 17C, 17N and 18 would be in from the control module 20underneath the scalp and then be connected to the electrodes placedbeneath the patient's cranium. Although FIG. 1 shows only four activeelectrodes 15A, 15B, 15C, 15N with connecting wires 17A, 17B, 17C, 17N,more than four active electrodes with connecting wires may be used withthe present invention. The electrode 16 (having the connecting wire 18)could be considered a common or indifferent electrode.

Throughout the detailed description of the present invention, theterminology “the electrodes 15A through 15N” is meant to include allelectrodes 15A, 15B, 15C, . . . to 15N, inclusive, where N may be anyinteger greater than or equal to 1. Similar terminology using the words“through” or “to” for other groups of objects (i.e., wires 17A through17N) will have a similar inclusive meaning.

Throughout FIGS. 1 through 5, inclusive, lines connecting boxes on blockdiagrams or on software flow charts will each be labeled with an elementnumber. Lines without arrows between boxes or other elements shallindicate a single wire. Lines with arrows connecting boxes or otherelements are used to represent any of the following:

1. A physical connection, namely a wire or group of wires (data bus)over which analog or digital signals may be sent.

2. A data stream sent from one hardware element to another. Data streamsinclude messages, analog or digital signals, commands, EEG information,and software downloads to change system operation and parameters.

3. A transfer of information between software modules. Such transfersinclude software subroutine calls with and without the passing ofparameters, and the reading and writing of memory locations.

In each case, the descriptive text herein will indicate each specificuse of a line with an arrow.

FIG. 2 is a block diagram of the implantable system 10 and the externalequipment 11. The wires 17A through 17N from the electrodes 15A through15N, and the wire 18 from the common electrode 16, are shown connectedto both an event detection sub-system 30 and a stimulation sub-system40. In one embodiment of the invention, it is also envisioned to use thecase of the control module 20 of FIG. 1 as the common (or indifferent)electrode 16. The wires 17A through 17N carry EEG signals 21A through21N from the electrodes 15A through 15N to the event detectionsub-system 30. The electrodes 15A through 15N can be energized by thestimulation sub-system 40 via the wires 17A through 17N to electricallystimulate the patient's brain using the stimulation signals 412A through412N respectively. Although the electrodes 15A through 15N and 16 shownhere are connected to both the event detection sub-system 30 and thestimulation sub-system 40, it should be apparent that a separate set ofelectrodes and associated wires could be used with each sub-system.Furthermore, it is envisioned that any one or more of the electrodes 15Athrough 15N could be electrically connected (i.e., shorted) to theelectrode 16 or to each other. This would be accomplished by appropriateswitching circuitry in the stimulation sub-system 40.

The event detection sub-system 30 receives the EEG signals 21A through21N (referenced to a system ground 19 connected to the wire 18 from thecommon electrode 16) and processes them to identify neurological eventssuch as an epileptic seizure or its precursor. A central processingsystem 50 with a central processor 51 and memory 55 acts to control andcoordinate all functions of the implantable system 10. A firstinterconnection 52 is used to transmit programming parameters andinstructions to the event detection sub-system 30 from the centralprocessing system 50. A second interconnection 53 is used to transmitsignals to the central processing system 50 identifying the detection ofa neurological event by the event detection sub-system 30. The secondinterconnection 53 is also used to transmit EEG and other related datafor storage in the memory 55.

When an event is detected by the event detection sub-system 30 (byprocessing such as that disclosed and described in U.S. Pat. No.6,016,449 to Fischell, et al., referenced above), the central processor51 can command the stimulation sub-system 40 via a third interconnection54 to transmit electrical signals to any one or more of the electrodes15A through 15N via the wires 17A through 17N. It is anticipated that,if appropriate, electrical signals 412A to 412N, inclusive, aretransmitted to certain locations in or near the brain, thereby abortingthe normal progression of an epileptic seizure. It may also be necessaryfor the stimulation sub-system 40 to temporarily disable the eventdetection sub-system 30 via a fourth interconnection 29 when stimulationis imminent so that the stimulation signals are not inadvertentlyinterpreted as a neurological event by the event detection sub-system30.

The stimulation sub-system 40 may also be engaged to perform continuousor periodic stimulation to the brain electrodes 15A through 15N,inclusive. In one embodiment of the invention, electrical stimulationfrom the stimulation sub-system 40 can include any of a wide range offrequencies from approximately 2 Hz to approximately 200 Hz. Details ofa signal generator capable of generating waveforms over such a frequencyrange are well known in the art of electronics design. In connectionwith the invention, it is, however, highly desirable to use stimulationat frequencies below 10 Hz. In particular, 5 Hz stimulation has beenshown to be inhibitory to ictal spikes in cat brains, and it is believedto be similarly effective in human patients. It is also known to be lesslikely for low frequency stimulation to induce epileptiform activity.

In one embodiment of the invention, the low-frequency stimulationapplied by an apparatus according to the invention comprises asubstantially sinusoidal waveform having little or no energy inhigher-frequency harmonics.

A power supply 90 provides power to each component of the system 10.Power supplies for comparable implantable devices such as heartpacemakers and heart defibrillators are well known in the art ofimplantable electronic devices. Such a power supply typically utilizes aprimary (non-rechargeable) storage battery with an associated d-c to d-cconverter to obtain any voltages required for the implantable system 10.However, it should be understood that in an alternative embodiment ofthe invention, the power supply could use a rechargeable battery that ischarged by means of a coil of wire in the control module 20 thatreceives energy by magnetic induction from an external coil that isplaced outside the patient but in close proximity to the control module20. The implanted coil of wire could also be located remotely fromcontrol module 20 but joined to it by electrical wires. Such technologyis well known from the rechargeable cardiac pacemaker. Furthermore, thesame pair of coils of wire could be used to provide power to theimplanted system 10 when it is desired to read out stored telemetry orreprogram some portion of the implanted system 10.

The central processing system 50 is connected to a data communicationsub-system 60, thereby allowing data stored in the memory 55 to beretrieved by the patient's physician via a wireless communication link72. An external data interface 70 can be directly connected to thephysician's workstation 80 via a traditional serial data connection 74(such as an RS-232 interface). Alternately, the serial connection may bemade trans-telephonically, via modems 85 and 750 and a phone line 75from the patient's home to the physician's workstation 80. Software inthe computer section of the physician's workstation 80 allows thephysician to read out a history of events detected by the implantablesystem 10, including EEG information before, during and after eachevent, as well as specific information relating to the detection of theevent, such as the time evolving energy spectrum of the patient's ECG.In a preferred embodiment of the invention, the physician's workstation80 also allows the physician to specify or alter any programmableparameters of the implantable system 10.

As shown in FIGS. 1 and 2, a buzzer 95 connected to the centralprocessor 51 via a link 92 can be used to notify the patient that aneurological event has occurred, the implanted system 10 is about todeliver stimulation, or that the implanted system 10 is not functioningproperly. In alternative embodiments, the buzzer could provide amechanical vibration (typically an acoustic signal) or an electricalstimulation “tickle,” either of which could be perceived by the patient.By placing the buzzer 95 near the ear and on the top of, below, orwithin a burr hole in the cranium, an acoustic signal emitted by thebuzzer 95 would be transmitted via bone conduction and detectable by thepatient's ear. This sound by itself can be an automatic means forstopping an epileptic seizure.

A real time clock 91 is used for timing and synchronizing variousportions of the implanted system 10 and also to enable the system toprovide the exact date and time corresponding to each neurological eventthat is detected by the implantable system 10 and recorded in the memory55. A fifth interconnection 96 is used to send data from the centralprocessor 51 to the real time clock 91 in order to set the correct dateand time in the clock 91.

The various interconnections between sub-systems (e.g., the illustratedinterconnections 29, 52, 53, 54, 56, 57, 92, 93 and 96) may be eitheranalog or digital, single wire or multiple wires (a “data bus”).

In an embodiment of the invention, the operation of the system 10 ofFIG. 2 for detecting and treating a neurological event such as anepileptic seizure would typically be as follows:

1. The event detection sub-system 30 continuously processes the EEGsignals 21A through 21N carried by the wires 17A through 17N from the Nelectrodes 15A through 15N.

2. When an event is detected, the event detection sub-system 30 notifiesthe central processor 51 via the second interconnection 53 that an eventhas occurred.

3. The central processor 51 then triggers the stimulation sub-system 40via the third interconnection 54 to electrically stimulate the patient'sbrain with low frequency electrical signals in order to stop theneurological event, using any one, several or all of the electrodes 15Athrough 15N.

4. The stimulation sub-system 40 also sends a signal via the fourthinterconnection 29 to the event detection sub-system 30 to disable eventdetection during stimulation to avoid an undesired input into the eventdetection sub-system 30.

5. The central processor system 50 will store EEG signals and eventrelated data received from the event detection sub-system 30 via thesecond interconnection 53 over a time from X minutes before the event toY minutes after the event for later analysis by the patient's physician.The value of X and Y may be set from as little as approximately 0.1minutes to as long as approximately 30 minutes.

6. The central processor 51 may generate a “buzz” to notify the patientthat an event has occurred by sending a signal via the link 92 to thebuzzer 95.

An alternative embodiment of the invention is shown in FIG. 3, whichillustrates the head of a patient showing a cross section of anon-invasive transcranial magnetic depolarizer system 100 as it would becontained within a helmet 111 of the type used by bicycle riders. Themagnetic depolarizer system 100 consists of a magnetic depolarizer coilassembly 112, a battery 114, electronic circuitry 115, a rechargingreceptacle 116 and interconnecting wires 117. The magnetic depolarizersystem 100 is contained within the helmet 111 by means of an elasticsupport 113 that passes between a front support 111A and a rear support111B. The purpose of the elastic support 113 is to keep the magneticdepolarizer coil 112 in comparatively tight contact with the patient'shead and at specific location relative to the patent's cerebral cortex.

FIG. 4A is a longitudinal cross section of the magnetic depolarizer 112of FIG. 3. The magnetic depolarizer coil assembly 112 consists of afirst coil 121 placed into a figure-eight configuration with a secondcoil 122. The two coils 121 and 122 are electrically connected in seriesin such a way as to create north magnetic poles 121A and 122A inessentially opposite directions when electric current is flowing throughthe coils 121 and 122. This orientation of coils 121 and 122 can producea comparatively strong magnetic field onto the cortex of the brain for adistance of a few centimeters beneath the cranium. If the magnetic fieldchanges rapidly in time, it produces an electric current in the brainthat can cause excited neurons to be depolarized. Ideally, slow TMS, at1 to 5 Hz, will transiently depress excitability. In an embodiment ofthe invention, the intensity of the magnetic field at the surface of thebrain should be between 0.1 and 10 Tesla. It is therefore an object ofthe present invention to use a device such as shown in FIG. 3 pulsed ata slow rate such as 1 or 2 Hz as an external means for treating aneurological disorder; preferably, this frequency is set and evaluatedby the patient's physician. Such a device could be worn all the time forchronic epileptics where periodic slow stimulation would act to keep thefocal region in a depressed condition, thus preventing a hyperexcitedstate associated with an epileptic seizure. For patients exhibiting anaura, the helmet could be put on as needed.

It should also be understood that the patient could use on or moreelastic bands (without a helmet) to place the magnetic depolarizer coilassembly 112 at an appropriate location onto his or her head.

FIG. 4B is a top view of the magnetic depolarizer coil assembly 112showing as dotted lines the outline of the coils 121 and 122. In bothFIGS. 3A and 3B, it is shown that the coils 121 and 122 could beencapsulated into a plastic housing 125. Furthermore, FIG. 3A shows amagnetic core 123 in the coil 121 and a separate magnetic core 124 inthe coil 122. These cores 123 and 124 are not required for the device toperform its intended purpose of generating a depolarizing electriccurrent within the cerebral cortex, but their presence facilitates thegeneration of a high-intensity magnetic field in the brain at a lowerlevel of electric current in the coils 121 and 122. To be effective atthe high frequency of the magnetic pulses that are used to stimulate thecortex, the cores 123 and 124 would typically be formed from powderediron or equivalent ferromagnetic material that has low eddy current andhysteresis losses.

Although FIGS. 4A and 4B show a race-track, figure eight type of designfor the magnetic depolarizer coil assembly 112, it should be understoodthat a simple cylindrical coil (and other shaped coils as well) with orwithout a ferromagnetic core could be used to generate the desiredtime-varying magnetic field.

FIG. 5 is a simplified electrical diagram of the magnetic depolarizersystem 100. The rechargeable battery 114 can be recharged through thereceptacle 116 by receiving a plug from a conventional AC adapter (notshown) that connects to a-c line voltage (e.g., 115 volts) and deliversan appropriate d-c voltage to recharge the rechargeable battery 114.When the patient is experiencing an aura of a migraine headache or othersymptoms of a neurological disorder, lie or she can throw the ON-OFFswitch 129 to the ON position. That would cause the d-c to d-c converter130 to activate and generate a high voltage for rapidly charging thecapacitor 126. When the control circuitry 128 senses that theappropriate voltage has been reached, it moves the switch 127 fromposition A to position B thus discharging the capacitor 126 through thecoils 121 and 122 of the magnetic depolarizer 112. As previouslydescribed, the coils 121 and 122 could have air cores or they could usemagnetically permeable cores 123 and 124. The control circuitry 128 canbe used to set the repetition rate for causing magnetic pulses to bedelivered. For example, a pulse from the capacitor might last for 70microseconds and could be repeated at the slow frequency rates betweenapproximately 0.1 and 10 Hz. A frequency of 1 Hz has been shown to beeffective in depolarizing brain neurons and may be ideal for somepatients. However, other patients might find other repetition rates tobe more effective. It is even possible that a single magnetic pulsehaving a time duration between 10 and 1,000 microseconds could be usedto stop an aura, thereby preventing the occurrence of a neurologicalevent.

In an embodiment of the invention, the TMS administered through anon-invasive magnetic depolarizer system according to the inventioncomprises a low-frequency signal (between approximately 0.1 Hz and 10Hz) modulated, via amplitude modulation or frequency modulation, onto acarrier frequency on the order of 100 Hz. It should be recognized thatthe carrier frequency given here is considered representative of abeneficial and advantageous carrier signal, and that various othercarrier frequencies and modulation schemes are possible. Variouswaveforms are also possible for both the TMS waveform and the carrierwaveform, including the substantially sinusoidal wave described above.Circuits capable of generating such stimulus signals are well known topractitioners skilled in the art of electronic circuit design.

Although FIGS. 3 and 5 show a battery operated magnetic depolarizersystem 100, the system 100 could be operated by plugging into areceptacle at (typically) 115 or 230 volts a-c. Such a system might ormight not use a battery as part of its circuitry.

Additional objects and advantages of the present invention will becomeapparent to those skilled in the art to which this invention relatesfrom the subsequent description of the preferred embodiments and theappended claims, taken in conjunction with the accompanying drawings.

The invention claimed is:
 1. An apparatus for treating a neurologicaldisorder of a patient through transcranial magnetic stimulation, theapparatus comprising: a positioning element configured to be placed onthe head of the patient; and a magnetic depolarizer system associatedwith the positioning element and comprising a magnetic depolarizer coilassembly, a power source, and control circuitry in operablecommunication with the power source and the magnetic depolarizer coilassembly, the control circuitry configured to cause the magneticdepolarizer coil assembly to deliver at least one magnetic field pulseto the patient, wherein the at least one magnetic field pulse isdelivered as a low frequency signal modulated on a carrier frequency,wherein the magnetic depolarizer coil assembly is disposed on thepositioning element at a location that places the magnetic depolarizercoil assembly adjacent the head of the patient when the positioningelement is placed on the head of the patient.
 2. The apparatus of claim1, wherein the control circuitry is further configured to set theduration of the at least one magnetic field pulse to between about 10microseconds and 1,000 microseconds.
 3. The apparatus of claim 1,wherein the at least one magnetic field pulse has a peak intensity of0.1 to 10 Tesla.
 4. The apparatus of claim 1, wherein the power sourcecomprises a rechargeable battery.
 5. The apparatus of claim 1, whereinthe at least one magnetic field pulse comprises a plurality of magneticfield pulses delivered at a rate of between approximately 0.1 and 10 Hz.6. The apparatus of claim 5, wherein each of the plurality of magneticfield pulses has a peak intensity of 0.1 to 10 Tesla.
 7. The apparatusof claim 1, further comprising an on/off switch associated with thepositioning element and in operable communication with the controlcircuitry, wherein the control circuitry is configured to generate theat least one magnetic field pulse in response to an activation of theon/off switch.
 8. The apparatus of claim 1, wherein the neurologicaldisorder comprises one or more of epilepsy, migraine headaches, andParkinson's disease.
 9. The apparatus of claim 1, wherein the carrierfrequency is on the order of 100 Hz and the low frequency signal isbetween approximately 0.1 Hz and 10 Hz.